Arterial aging—hemodynamic changes and therapeutic options

Abstract

Arterial aging can be attributed to two different pathophysiological changes--increase in arterial stiffness and disturbed wave reflections. The capacity of the aorta to absorb the force exerted by the left ventricular ejection and dampen pulsatile flow becomes diminished with advancing age, owing to the progressive hardening of the arterial wall. These changes contribute to increase blood pressure, mainly systolic blood pressure and pulse pressure, which can trigger cardiovascular events. Understanding the pulsatile arterial hemodynamics that elevate cardiovascular risk has led to the use of pharmacological therapies, which prevent arterial stiffness and reduce wave reflections, and improve cardiovascular morbidity and mortality. Antifibrotic agents, such as those that block the renin-angiotensin-aldosterone pathway, are often given in association with diuretics, calcium-channel blockers, or both, but not with standard beta-blockers. Consistent reductions in cardiovascular outcomes obtained using these agents can be predicted through noninvasive measurements of central systolic blood pressure and pulse pressure.